Cardiomyocyte-Restricted Overexpression of Endothelial Nitric Oxide Synthase ( <i>NOS3</i> ) Attenuates β-Adrenergic Stimulation and Reinforces Vagal Inhibition of Cardiac Contraction

Abstract

Moderate overexpression of NOS3, targeted to caveolae in murine cardiomyocytes, potentiates the postsynaptic muscarinic response and attenuates the effect of high concentrations of catecholamines. Cardiomyocyte NOS3 may represent a promising therapeutic target to restore the sympathovagal balance and protect the heart against arrhythmia.